CHRONIC EXPOSURE OF CANCER-PRONE MICE TO LOW-LEVEL 2450 MHZ RADIOFREQUENCY RADIATION

The purpose of this study was to determine whether chronic, low-level exposure of mammary-tumor-prone mice to 2450 MHz radiofrequency radiat ion (RFR) promotes an earlier onset (decreased latency), a greater tot al incidence, or a faster growth rate of mammary tumors. One hundred C 3H/HeJ mice were exposed in circularly polarized waveguides (CWG) for 18 months (20 h/day, 7 days/wk) to continuous-wave, 2450 MHz RFR at a whole body average specific absorption rate (SAR) of 0.3 W/kg; 100 mic e were sham exposed. Before exposure, SARs were determined calorimetri cally; during experimentation, SARs were monitored by differential pow er measurement. All animals were visually inspected twice daily and we re removed from the CWG cages for a weekly inspection, palpation, and weighing. From the time of detection, tumor size was measured weekly. Animals that died spontaneously, became moribund, or mere killed after 18 months of exposure were completely necropsied; tissues were fixed and subjected to histopathological evaluations. Results showed no sign ificant difference in weight profiles between sham-irradiated and irra diated mice. Concerning mammary carcinomas, there was no significant d ifference between groups with respect to palpated tumor incidence (sha m = 52%; irradiated = 44%), latency to tumor onset (sham = 62.3 +/- 1. 2 wk; irradiated = 64.0 +/- 1.6 wk), and rate of tumor growth. In gene ral, histopathological examination revealed no significant differences in numbers of malignant, metastatic, or benign neoplasms between the two groups; a significantly greater incidence of alveolar-bronchiolar adenoma in the sham-irradiated mice was the only exception. In additio n, survival analysis showed no significant difference in cumulative pe rcent survival between sham and irradiated animals. Thus, results indi cate that under the conditions of this study, long-term, tow-level exp osure of mammary-tumor-prone mice to 2450 MHz RFR did not affect mamma ry tumor incidence, latency to tumor onset, tumor growth rate, or anim al longevity when compared with sham-irradiated controls. (C) 1998 Wil ey-Liss, Inc.